Reading disability (RD), also known as developmental dyslexia and also known as dyslexia, is one of the most common of the complex neurobehavioral disorders, with prevalence rates ranging from 5 to 17 percent (1). It is characterized by an impairment of reading ability in subjects with normal intelligence and adequate educational opportunities. A range of neuroimaging studies, including diffusion tensor and functional magnetic resonance imaging, show that dyslexics have altered brain activation patterns compared to fluent readers when challenged with reading tasks (2). Partial remediation in language processing deficits results in improved reading, ameliorates disrupted function in brain regions associated with phonologic processing, and produces additional compensatory activation in other brain areas (3). These studies also implicate specific brain locations where genes integral to reading and language are expressed, and which likely are altered in RD.
Over the past 30 years clinical studies have shown that up to 50% of children of dyslexic parents, 50% of siblings of dyslexics, and 50% of parents of dyslexic children are affected (4). Estimates of heritability range from 44 to 75% (5). The first RD susceptibility region, DYX1, was reported on chromosome 15 in 1983 (6). Subsequently, loci were described on chromosomes 1, 2p15-16, 3p13, 6p (7-21), 6q, 7q32, 11, 15q21, and 18p11.2. It is still unclear which and/or how many genes contribute to RD and additional information would be useful for developing diagnostic, preventive and therapeutic approaches to this disorder.